Consistent with this interpretation, scrib-mediated impairment to Hippo signalling has been shown to be atypical Protein Kinase C (aPKC)-dependent, since it is rescued by expressing a kinase dead dominant negative (DN) version of aPKC (aPKCDN) within the mutant tissue [31], and similarly, expressing aPKCDN in scrib−+ab tumours also curtailed tumour overgrowth (Figure S15). Here, SCRIB is linked to neoplasm.